1
40
10
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2018.01.013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2018.01.013</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
159-171
Volume
116
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nrf2/ARE pathway attenuates oxidative and apoptotic response in human osteoarthritis chondrocytes by activating ERK1/2/ELK1-P70S6K-P90RSK signaling axis.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-02
Subject
The topic of the resource
Humans; *Apoptosis; *Apoptosis; *ERK1/2; *Nrf2; *Osteoarthritis; *Redox; Oxidative Stress; Osteoarthritis/*metabolism; NF-E2-Related Factor 2/genetics/*metabolism; Up-Regulation; MAP Kinase Signaling System; Chondrocytes/*physiology; Caspases/metabolism; Cells; Cultured; 70-kDa/metabolism; Ribosomal Protein S6 Kinases; Carboxylic Ester Hydrolases/metabolism; ets-Domain Protein Elk-1/metabolism; Interleukin-1beta/immunology; 90-kDa/metabolism
Creator
An entity primarily responsible for making the resource
Khan Nazir M; Ahmad Imran; Haqqi Tariq M
Description
An account of the resource
Nrf2, a redox regulated transcription factor, has recently been shown to play a role in cartilage integrity but the mechanism remains largely unknown. Osteoarthritis (OA) is a multifactorial disease in which focal degradation of cartilage occurs. Here, we studied whether Nrf2 exerts chondroprotective effects by suppressing the oxidative stress and apoptosis in IL-1beta stimulated human OA chondrocytes. Expression of Nrf2 and its target genes HO-1, NQO1 and SOD2 was significantly high in OA cartilage compared to normal cartilage and was also higher in damaged area compared to smooth area of OA cartilage of the same patient. Human chondrocytes treated with IL-1beta resulted in robust Nrf2/ARE reporter activity, which was inhibited by pretreatment with antioxidants indicating that Nrf2 activity was due to IL-1beta-induced ROS generation. Ectopic expression of Nrf2 significantly suppressed the IL-1beta-induced generation of ROS while Nrf2 knockdown significantly increased the basal as well as
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2018.01.013" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2018.01.013</a>
*Apoptosis
*ERK1/2
*Nrf2
*OSTEOARTHRITIS
*Redox
2018
70-kDa/metabolism
90-kDa/metabolism
Ahmad Imran
Carboxylic Ester Hydrolases/metabolism
Caspases/metabolism
Cells
Chondrocytes/*physiology
Cultured
ets-Domain Protein Elk-1/metabolism
Free radical biology & medicine
Haqqi Tariq M
Humans
Interleukin-1beta/immunology
Khan Nazir M
MAP Kinase Signaling System
NF-E2-Related Factor 2/genetics/*metabolism
Osteoarthritis/*metabolism
Oxidative Stress
Ribosomal Protein S6 Kinases
Up-Regulation
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2018.01.013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2018.01.013</a>
Pages
159–171
Volume
116
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Nrf2/ARE pathway attenuates oxidative and apoptotic response in human osteoarthritis chondrocytes by activating ERK1/2/ELK1-P70S6K-P90RSK signaling axis.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-02
Subject
The topic of the resource
*Apoptosis; *ERK1/2; *Nrf2; *Osteoarthritis; *Redox
Creator
An entity primarily responsible for making the resource
Khan Nazir M; Ahmad Imran; Haqqi Tariq M
Description
An account of the resource
Nrf2, a redox regulated transcription factor, has recently been shown to play a role in cartilage integrity but the mechanism remains largely unknown. Osteoarthritis (OA) is a multifactorial disease in which focal degradation of cartilage occurs. Here, we studied whether Nrf2 exerts chondroprotective effects by suppressing the oxidative stress and apoptosis in IL-1beta stimulated human OA chondrocytes. Expression of Nrf2 and its target genes HO-1, NQO1 and SOD2 was significantly high in OA cartilage compared to normal cartilage and was also higher in damaged area compared to smooth area of OA cartilage of the same patient. Human chondrocytes treated with IL-1beta resulted in robust Nrf2/ARE reporter activity, which was inhibited by pretreatment with antioxidants indicating that Nrf2 activity was due to IL-1beta-induced ROS generation. Ectopic expression of Nrf2 significantly suppressed the IL-1beta-induced generation of ROS while Nrf2 knockdown significantly increased the basal as well as
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2018.01.013" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2018.01.013</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Apoptosis
*ERK1/2
*Nrf2
*OSTEOARTHRITIS
*Redox
2018
Ahmad Imran
Department of Anatomy & Neurobiology
Free radical biology & medicine
Haqqi Tariq M
Khan Nazir M
NEOMED College of Medicine
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.10.373" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2017.10.373</a>
Pages
461–469
Volume
113
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Increased serotransferrin and ceruloplasmin turnover in diet-controlled patients with type 2 diabetes.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
*Ceruloplasmin; *Deamidation; *Heavy water metabolic labeling; *High resolution mass spectrometry; *Iron metabolism; *LC-MS/MS; *Non-enzymatic glycation; *Oxidative stress; *Protein Processing; *Proteome dynamics; *Serotransferrin; *Type 2 diabetes mellitus; Adult; Amino Acid Sequence; Case-Control Studies; Ceruloplasmin/genetics/*metabolism; Deuterium/metabolism; Diabetes Mellitus; Diabetic; Diet; Female; Gene Expression Regulation; Glycated Hemoglobin A/genetics/metabolism; Glycosylation; Humans; Iron/*metabolism; Isotope Labeling; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Post-Translational; Proteolysis; Transferrin/genetics/*metabolism; Type 2/diet therapy/genetics/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Golizeh Makan; Lee Kwangwon; Ilchenko Serguei; Osme Abdullah; Bena James; Sadygov Rovshan G; Kashyap Sangeeta R; Kasumov Takhar
Description
An account of the resource
Type 2 diabetes mellitus (T2DM) is associated with oxidative stress and perturbed iron metabolism. Serotransferrin (Trf) and ceruloplasmin (Cp) are two key proteins involved in iron metabolism and anti-oxidant defense. Non-enzymatic glycation and oxidative modification of plasma proteins are known to occur under hyperglycemia and oxidative stress. In this study, shotgun proteomics and (2)H2O-based metabolic labeling were used to characterize post-translational modifications and assess the kinetics of Trf and Cp in T2DM patients and matched controls in vivo. Six early lysine (Amadori) and one advanced arginine glycation were detected in Trf. No glycation, but five asparagine deamidations, were found in Cp. T2DM patients had increased fractional catabolic rates of both Trf and Cp that correlated with HbA1c (p \textless 0.05). The glycated Trf population was subject to an even faster degradation compared to the total Trf pool, suggesting that hyperglycemia contributed to an increased Trf degradation in T2DM patients. Enhanced production of Trf and Cp kept their levels stable. The changes in Trf and Cp turnover were associated with increased systemic oxidative stress without any alteration in iron status in T2DM. These findings can help better understand the potential role of altered Trf and Cp metabolism in the pathogenesis of T2DM and other diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.10.373" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2017.10.373</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Ceruloplasmin
*Deamidation
*Heavy water metabolic labeling
*High resolution mass spectrometry
*Iron metabolism
*LC-MS/MS
*Non-enzymatic glycation
*Oxidative Stress
*Protein Processing
*Proteome dynamics
*Serotransferrin
*Type 2 diabetes mellitus
2017
Adult
Amino Acid Sequence
Bena James
Case-Control Studies
Ceruloplasmin/genetics/*metabolism
Department of Pharmaceutical Sciences
Deuterium/metabolism
Diabetes Mellitus
Diabetic
Diet
Female
Free radical biology & medicine
Gene Expression Regulation
Glycated Hemoglobin A/genetics/metabolism
Glycosylation
Golizeh Makan
Humans
Ilchenko Serguei
Iron/*metabolism
Isotope Labeling
Kashyap Sangeeta R
Kasumov Takhar
Lee Kwangwon
Male
Middle Aged
NEOMED College of Pharmacy
Osme Abdullah
Oxidation-Reduction
Oxidative Stress
Post-Translational
Proteolysis
Sadygov Rovshan G
Transferrin/genetics/*metabolism
Type 2/diet therapy/genetics/*metabolism/pathology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.04.022" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2017.04.022</a>
Pages
595–609
Volume
108
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Differential protein acetylation assists import of excess SOD2 into mitochondria and mediates SOD2 aggregation associated with cardiac hypertrophy in the murine
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-07
Subject
The topic of the resource
*Cardiac-specific transgenic mouse; *Mitochondria; *Mitochondrial translocation; *Protein acetylation; *Protein aggregation; *SOD2; Acetylation; Animals; Cardiomegaly/*metabolism; Cytosol/*metabolism; Heart/*physiology; Mice; Mitochondria/*metabolism; Pathological; Post-Translational; Protein Aggregation; Protein Folding; Protein Processing; Protein Transport; Reactive Oxygen Species/metabolism; Sirtuin 3/metabolism; Superoxide Dismutase/genetics/*metabolism; Transgenic
Creator
An entity primarily responsible for making the resource
Zhang Liwen; Chen Chwen-Lih; Kang Patrick T; Jin Zhicheng; Chen Yeong-Renn
Description
An account of the resource
SOD2 is the primary antioxidant enzyme neutralizing (*)O2(-) in mitochondria. Cardiac-specific SOD2 overexpression (SOD2-tg) induces supernormal function and cardiac hypertrophy in the mouse heart. However, the reductive stress imposed by SOD2 overexpression results in protein aggregation of SOD2 pentamers and differential hyperacetylation of SOD2 in the mitochondria and cytosol. Here, we studied SOD2 acetylation in SOD2-tg and wild-type mouse hearts. LC-MS/MS analysis indicated the presence of four acetylated lysines in matrix SOD2 and nine acetylated lysines in cytosolic SOD2 from the SOD2-tg heart. However, only one specific acetylated lysine residue was detected in the mitochondria of the wild-type heart, which was consistent with Sirt3 downregulation in the SOD2-tg heart. LC-MS/MS further detected hyperacetylated SOD2 with a signaling peptide in the mitochondrial inner membrane and matrix of the SOD2-tg heart, indicating partial arrest of the SOD2 precursor in the membrane during translocation into the mitochondria. Upregulation of HSP 70 and cytosolic HSP 60 enabled the translocation of excess SOD2 into mitochondria. In vitro acetylation of matrix SOD2 with Ac2O deaggregated pentameric SOD2, restored the profile of cytosolic SOD2 hyperacetylation, and decreased matrix SOD2 activity. As revealed by 3D structure, acetylation of K89, K134, and K154 of cytosolic SOD2 induces unfolding of the tertiary structure and breaking of the salt bridges that are important for the quaternary structure, suggesting that hyperacetylation and HSP 70 upregulation maintain the unfolded status of SOD2 in the cytosol and mediate the import of SOD2 across the membrane. Downregulation of Sirt3, HSP 60, and presequence protease in the mitochondria of the SOD2-tg heart promoted protein misfolding that led to pentameric aggregation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.04.022" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2017.04.022</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cardiac-specific transgenic mouse
*Mitochondria
*Mitochondrial translocation
*Protein acetylation
*Protein aggregation
*SOD2
2017
Acetylation
Animals
Cardiomegaly/*metabolism
Chen Chwen-Lih
Chen Yeong-Renn
Cytosol/*metabolism
Department of Integrative Medical Sciences
Free radical biology & medicine
Heart/*physiology
Jin Zhicheng
Kang Patrick T
Mice
Mitochondria/*metabolism
NEOMED College of Medicine
Pathological
Post-Translational
Protein Aggregation
Protein Folding
Protein Processing
Protein Transport
Reactive Oxygen Species/metabolism
Sirtuin 3/metabolism
Superoxide Dismutase/genetics/*metabolism
Transgenic
Zhang Liwen
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.02.041" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2017.02.041</a>
Pages
288–301
Volume
106
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Wogonin, a plant derived small molecule, exerts potent anti-inflammatory and chondroprotective effects through the activation of ROS/ERK/Nrf2 signaling pathways in human Osteoarthritis chondrocytes.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-05
Subject
The topic of the resource
*ERK1/2; *Nrf2; *Osteoarthritis; *Redox; *Wogonin; Anti-Inflammatory Agents/administration & dosage; Chondrocytes/drug effects/pathology; Flavanones/*administration & dosage; Gene Expression Regulation/drug effects; Humans; Inflammation/*drug therapy/metabolism/pathology; Kelch-Like ECH-Associated Protein 1/chemistry/*genetics/metabolism; MAP Kinase Signaling System/drug effects; Molecular Docking Simulation; NF-E2-Related Factor 2/antagonists & inhibitors/chemistry/*genetics/metabolism; Osteoarthritis/*drug therapy/metabolism/pathology; Protein Binding; Reactive Oxygen Species/metabolism; Signal Transduction/drug effects
Creator
An entity primarily responsible for making the resource
Khan Nazir M; Haseeb Abdul; Ansari Mohammad Y; Devarapalli Pratap; Haynie Sara; Haqqi Tariq M
Description
An account of the resource
Osteoarthritis (OA), characterized by progressive destruction of articular cartilage, is the most common form of human arthritis. Here, we evaluated the potential chondroprotective and anti-inflammatory effects of Wogonin, a naturally occurring flavonoid, in IL-1beta-stimulated human OA chondrocytes and cartilage explants. Wogonin completely suppressed the expression and production of inflammatory mediators including IL-6, COX-2, PGE2, iNOS and NO in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.02.041" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2017.02.041</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*ERK1/2
*Nrf2
*OSTEOARTHRITIS
*Redox
*Wogonin
2017
Ansari Mohammad Y
Anti-Inflammatory Agents/administration & dosage
Chondrocytes/drug effects/pathology
Department of Anatomy & Neurobiology
Devarapalli Pratap
Flavanones/*administration & dosage
Free radical biology & medicine
Gene Expression Regulation/drug effects
Haqqi Tariq M
Haseeb Abdul
Haynie Sara
Humans
Inflammation/*drug therapy/metabolism/pathology
Kelch-Like ECH-Associated Protein 1/chemistry/*genetics/metabolism
Khan Nazir M
MAP Kinase Signaling System/drug effects
Molecular Docking Simulation
NEOMED College of Medicine
NF-E2-Related Factor 2/antagonists & inhibitors/chemistry/*genetics/metabolism
Osteoarthritis/*drug therapy/metabolism/pathology
Protein Binding
Reactive Oxygen Species/metabolism
Signal Transduction/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
Vasodilation/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.03.032" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.03.032</a>
Pages
13–21
Volume
96
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A Western diet induced NAFLD in LDLR(-/)(-) mice is associated with reduced hepatic glutathione synthesis.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-07
Subject
The topic of the resource
*Flux; *Glutathione; *Heavy water; *Mass spectrometer; *NAFLD; *NASH; *Oxidative stress; *Western Diet; Animal; Animals; Antioxidants/metabolism; Diet; Disease Models; Glutathione/blood/*metabolism; Humans; LDL/blood/*genetics/metabolism; Liver/*metabolism/pathology; Mice; Non-alcoholic Fatty Liver Disease/blood/*genetics/pathology; Oxidative Stress/genetics; Receptors; Western/adverse effects
Creator
An entity primarily responsible for making the resource
Li Ling; Zhang Guo-Fang; Lee Kwangwon; Lopez Rocio; Previs Stephen F; Willard Belinda; McCullough Arthur; Kasumov Takhar
Description
An account of the resource
Oxidative stress plays a key role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Glutathione is the major anti-oxidant involved in cellular oxidative defense, however there are currently no simple non-invasive methods for assessing hepatic glutathione metabolism in patients with NAFLD. As a primary source of plasma glutathione, liver plays an important role in interorgan glutathione homeostasis. In this study, we have tested the hypothesis that measurements of plasma glutathione turnover could be used to assess the hepatic glutathione metabolism in LDLR(-/)(-) mice, a mouse model of diet-induced NAFLD. Mice were fed a standard low fat diet (LFD) or a high fat diet containing cholesterol (a Western type diet (WD)). The kinetics of hepatic and plasma glutathione were quantified using the (2)H2O metabolic labeling approach. Our results show that a WD leads to reduced fractional synthesis rates (FSR) of hepatic (25%/h in LFD vs. 18%/h in WD, P\textless0.05) and plasma glutathione (43%/h in LFD vs. 21%/h in WD, P\textless0.05), without any significant effect on their absolute production rates (PRs). WD-induced concordant changes in both hepatic and plasma glutathione turnover suggest that the plasma glutathione turnover measurements could be used to assess hepatic glutathione metabolism. The safety, simplicity, and low cost of the (2)H2O-based glutathione turnover approach suggest that this method has the potential for non-invasive probing of hepatic glutathione metabolism in patients with NAFLD and other diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.03.032" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.03.032</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Flux
*Glutathione
*Heavy water
*Mass spectrometer
*NAFLD
*NASH
*Oxidative Stress
*Western Diet
2016
Animal
Animals
Antioxidants/metabolism
Department of Pharmaceutical Sciences
Diet
Disease Models
Free radical biology & medicine
Glutathione/blood/*metabolism
Humans
Kasumov Takhar
LDL/blood/*genetics/metabolism
Lee Kwangwon
Li Ling
Liver/*metabolism/pathology
Lopez Rocio
McCullough Arthur
Mice
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease/blood/*genetics/pathology
Oxidative Stress/genetics
Previs Stephen F
Receptors
Western/adverse effects
Willard Belinda
Zhang Guo-Fang
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2014.11.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2014.11.016</a>
Pages
56–68
Volume
79
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Increased mitochondrial prooxidant activity mediates up-regulation of Complex I
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-02
Subject
The topic of the resource
*Up-Regulation; Animals; Complex I; Electron Spin Resonance Spectroscopy; eNOS(-/-) murine heart; Glutathione/*metabolism; Heart/*metabolism; Knockout; Mice; Mitochondria; Myocardium/enzymology/*metabolism; Nitric Oxide Synthase Type III/genetics/*metabolism; Oxidation-Reduction; Oxidative stress; Protein thiyl radical; Reactive Oxygen Species/*metabolism; S-Glutathionylation; Superoxides/metabolism
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Chen Chwen-Lih; Chen Yeong-Renn
Description
An account of the resource
In response to oxidative stress, mitochondrial Complex I is reversibly
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2014.11.016" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2014.11.016</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Up-Regulation
2015
Animals
Chen Chwen-Lih
Chen Yeong-Renn
Complex I
Department of Integrative Medical Sciences
Electron Spin Resonance Spectroscopy
eNOS(-/-) murine heart
Free radical biology & medicine
Glutathione/*metabolism
Heart/*metabolism
Kang Patrick T
Knockout
Mice
Mitochondria
Myocardium/enzymology/*metabolism
NEOMED College of Medicine
Nitric Oxide Synthase Type III/genetics/*metabolism
Oxidation-Reduction
Oxidative Stress
Protein thiyl radical
Reactive Oxygen Species/*metabolism
S-Glutathionylation
Superoxides/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2012.05.025" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2012.05.025</a>
Pages
962–973
Issue
4
Volume
53
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Protein thiyl radical mediates S-glutathionylation of complex I.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-08
Subject
The topic of the resource
*Oxidative Stress; Amino Acid Motifs; Amino Acid Sequence; Animals; Binding Sites; Cattle; Cell Line; Cyclic N-Oxides/chemistry/pharmacology; Cysteine/chemistry/*metabolism; Electron Transport Complex I/chemistry/*metabolism; Free Radical Scavengers/chemistry/pharmacology; Free Radicals/chemistry/*metabolism; Glutathione/chemistry/*metabolism; Heart/enzymology/metabolism; Mice; Mitochondria; Models; Molecular; Molecular Sequence Data; Muscle Cells/drug effects/metabolism; Onium Compounds/pharmacology; Peptide Fragments/chemistry; Peptide Mapping; Protein; Rats; Rotenone/pharmacology; Structural Homology; Superoxides/metabolism
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Zhang Liwen; Chen Chwen-Lih; Chen Jingfeng; Green Kari B; Chen Yeong-Renn
Description
An account of the resource
Complex I is a critical site of O(2)(*-) production and the major host of reactive protein thiols in mitochondria. In response to oxidative stress, complex I protein thiols at the 51- and 75-kDa subunits are reversibly
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2012.05.025" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2012.05.025</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Oxidative Stress
2012
Amino Acid Motifs
Amino Acid Sequence
Animals
Binding Sites
Cattle
Cell Line
Chen Chwen-Lih
Chen Jingfeng
Chen Yeong-Renn
Cyclic N-Oxides/chemistry/pharmacology
Cysteine/chemistry/*metabolism
Department of Integrative Medical Sciences
Electron Transport Complex I/chemistry/*metabolism
Free radical biology & medicine
Free Radical Scavengers/chemistry/pharmacology
Free Radicals/chemistry/*metabolism
Glutathione/chemistry/*metabolism
Green Kari B
Heart/enzymology/metabolism
Kang Patrick T
Mice
Mitochondria
Models
Molecular
Molecular Sequence Data
Muscle Cells/drug effects/metabolism
NEOMED College of Medicine
Onium Compounds/pharmacology
Peptide Fragments/chemistry
Peptide Mapping
Protein
Rats
Rotenone/pharmacology
Structural Homology
Superoxides/metabolism
Zhang Liwen
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2011.05.034</a>
Pages
876–883
Issue
4
Volume
51
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Vitamin B12 protects against superoxide-induced cell injury in human aortic endothelial cells.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
Aorta/pathology; Apoptosis/drug effects; Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology; Cell Line; Cell Survival/drug effects; Cytoprotection; Endothelium; Free Radical Scavengers/*pharmacology; Humans; Mitochondria/drug effects/metabolism/pathology; Oxidative Stress/drug effects; Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology; Superoxides/metabolism; Vascular/*drug effects/metabolism/pathology; Vitamin B 12/*pharmacology; Vitamin B Complex/*pharmacology
Creator
An entity primarily responsible for making the resource
Moreira Edward S; Brasch Nicola E; Yun June
Description
An account of the resource
Superoxide (O(2)(*-)) is implicated in inflammatory states including arteriosclerosis and ischemia-reperfusion injury. Cobalamin (Cbl) supplementation is beneficial for treating many inflammatory diseases and also provides protection in oxidative-stress-associated pathologies. Reduced Cbl reacts with O(2)(*-) at rates approaching that of superoxide dismutase (SOD), suggesting a plausible mechanism for its anti-inflammatory properties. Elevated homocysteine (Hcy) is an independent risk factor for cardiovascular disease and endothelial dysfunction. Hcy increases O(2)(*-) levels in human aortic endothelial cells (HAEC). Here, we explore the protective effects of Cbl in HAEC exposed to various O(2)(*-) sources, including increased Hcy levels. Hcy increased O(2)(*-) levels (1.6-fold) in HAEC, concomitant with a 20% reduction in cell viability and a 1.5-fold increase in apoptotic death. Pretreatment of HAEC with physiologically relevant concentrations of cyanocobalamin (CNCbl) (10-50nM) prevented Hcy-induced increases in O(2)(*-) and cell death. CNCbl inhibited both Hcy and rotenone-induced mitochondrial O(2)(*-) production. Similarly, HAEC challenged with paraquat showed a 1.5-fold increase in O(2)(*-) levels and a 30% decrease in cell viability, both of which were prevented with CNCbl pretreatment. CNCbl also attenuated elevated O(2)(*-) levels after exposure of cells to a Cu/Zn-SOD inhibitor. Our data suggest that Cbl acts as an efficient intracellular O(2)(*-) scavenger.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2011.05.034</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
Aorta/pathology
Apoptosis/drug effects
Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology
Brasch Nicola E
Cell Line
Cell Survival/drug effects
Cytoprotection
Department of Integrative Medical Sciences
Endothelium
Free radical biology & medicine
Free Radical Scavengers/*pharmacology
Humans
Mitochondria/drug effects/metabolism/pathology
Moreira Edward S
NEOMED College of Medicine
Oxidative Stress/drug effects
Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology
Superoxides/metabolism
Vascular/*drug effects/metabolism/pathology
Vitamin B 12/*pharmacology
Vitamin B Complex/*pharmacology
Yun June